β-Endorphin enhances concanavalin-A-stimulated calcium mobilization by murine splenic T cells

Nahid A. Shahabi, Wyrta Heagy, Burt Sharp

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Intracellular calcium mobilization is an important early event involved in T cell activation. The endogenous opioid peptide β-endorphin is known to modulate immune functions that depend on T cell activation, therefore its effect on intracellular calcium mobilization was investigated. The intracellular calcium concentration ([Ca2+](i)) of T cell-enriched splenocytes was measured by flow cytofluorometric analysis using the calcium- sensitive dye, Fluo-3. By gating on the T cell marker, Thy-1, a 95%-pure population oft cells was identified for study. Cells preincubated with β- endorphin showed significantly enhanced [Ca2+](i) responses to the mitogen, Concanavalin A (Con A). This was detectable with concentrations of β- endorphin as low as 10-13 M; maximal enhancement required 10-10 to 10- 9 M doses. The efficacy of β-endorphin was dependent on the duration of pretreatment. β-Endorphin amplified the Con A-induced increase in [Ca2+](i) by reducing the lag time for the response to Con A and by increasing the mean [Ca2+](i) of the cells. N-Ac-β-endorphin, which shows minimal potency at neuronal opiate receptors, was unable to substitute for β-endorphin. Naltrindole, a highly selective δ opiate receptor antagonist, inhibited the action of β-endorphin, whereas a selective μ opiate receptor antagonist was ineffective. Although less potent than β-endorphin, the δ opiate receptor agonist D-Ala2-D-Leu5-enkephalin also significantly enhanced [Ca2+](i) responses. In summary, concentrations of β-endorphin, within the physiological range found in the systemic circulation, modulate the increase in T cell [Ca2+](i) induced by Con A. Both the efficacy of D- Ala2-D-Leu5-enkephalin alone and the antagonism of β-endorphin by naltrindole suggest that a δ-type opiate receptor may mediate these effects.

Original languageEnglish (US)
Pages (from-to)3386-3393
Number of pages8
JournalEndocrinology
Volume137
Issue number8
DOIs
StatePublished - Jan 1 1996

Fingerprint

Endorphins
Concanavalin A
Calcium
T-Lymphocytes
Opioid Receptors
naltrindole
Opioid Peptides
Mitogens
Coloring Agents

All Science Journal Classification (ASJC) codes

  • Endocrinology

Cite this

β-Endorphin enhances concanavalin-A-stimulated calcium mobilization by murine splenic T cells. / Shahabi, Nahid A.; Heagy, Wyrta; Sharp, Burt.

In: Endocrinology, Vol. 137, No. 8, 01.01.1996, p. 3386-3393.

Research output: Contribution to journalArticle

Shahabi, Nahid A. ; Heagy, Wyrta ; Sharp, Burt. / β-Endorphin enhances concanavalin-A-stimulated calcium mobilization by murine splenic T cells. In: Endocrinology. 1996 ; Vol. 137, No. 8. pp. 3386-3393.
@article{82a772a178684e1c92ebfe39e7188b38,
title = "β-Endorphin enhances concanavalin-A-stimulated calcium mobilization by murine splenic T cells",
abstract = "Intracellular calcium mobilization is an important early event involved in T cell activation. The endogenous opioid peptide β-endorphin is known to modulate immune functions that depend on T cell activation, therefore its effect on intracellular calcium mobilization was investigated. The intracellular calcium concentration ([Ca2+](i)) of T cell-enriched splenocytes was measured by flow cytofluorometric analysis using the calcium- sensitive dye, Fluo-3. By gating on the T cell marker, Thy-1, a 95{\%}-pure population oft cells was identified for study. Cells preincubated with β- endorphin showed significantly enhanced [Ca2+](i) responses to the mitogen, Concanavalin A (Con A). This was detectable with concentrations of β- endorphin as low as 10-13 M; maximal enhancement required 10-10 to 10- 9 M doses. The efficacy of β-endorphin was dependent on the duration of pretreatment. β-Endorphin amplified the Con A-induced increase in [Ca2+](i) by reducing the lag time for the response to Con A and by increasing the mean [Ca2+](i) of the cells. N-Ac-β-endorphin, which shows minimal potency at neuronal opiate receptors, was unable to substitute for β-endorphin. Naltrindole, a highly selective δ opiate receptor antagonist, inhibited the action of β-endorphin, whereas a selective μ opiate receptor antagonist was ineffective. Although less potent than β-endorphin, the δ opiate receptor agonist D-Ala2-D-Leu5-enkephalin also significantly enhanced [Ca2+](i) responses. In summary, concentrations of β-endorphin, within the physiological range found in the systemic circulation, modulate the increase in T cell [Ca2+](i) induced by Con A. Both the efficacy of D- Ala2-D-Leu5-enkephalin alone and the antagonism of β-endorphin by naltrindole suggest that a δ-type opiate receptor may mediate these effects.",
author = "Shahabi, {Nahid A.} and Wyrta Heagy and Burt Sharp",
year = "1996",
month = "1",
day = "1",
doi = "10.1210/endo.137.8.8754765",
language = "English (US)",
volume = "137",
pages = "3386--3393",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "The Endocrine Society",
number = "8",

}

TY - JOUR

T1 - β-Endorphin enhances concanavalin-A-stimulated calcium mobilization by murine splenic T cells

AU - Shahabi, Nahid A.

AU - Heagy, Wyrta

AU - Sharp, Burt

PY - 1996/1/1

Y1 - 1996/1/1

N2 - Intracellular calcium mobilization is an important early event involved in T cell activation. The endogenous opioid peptide β-endorphin is known to modulate immune functions that depend on T cell activation, therefore its effect on intracellular calcium mobilization was investigated. The intracellular calcium concentration ([Ca2+](i)) of T cell-enriched splenocytes was measured by flow cytofluorometric analysis using the calcium- sensitive dye, Fluo-3. By gating on the T cell marker, Thy-1, a 95%-pure population oft cells was identified for study. Cells preincubated with β- endorphin showed significantly enhanced [Ca2+](i) responses to the mitogen, Concanavalin A (Con A). This was detectable with concentrations of β- endorphin as low as 10-13 M; maximal enhancement required 10-10 to 10- 9 M doses. The efficacy of β-endorphin was dependent on the duration of pretreatment. β-Endorphin amplified the Con A-induced increase in [Ca2+](i) by reducing the lag time for the response to Con A and by increasing the mean [Ca2+](i) of the cells. N-Ac-β-endorphin, which shows minimal potency at neuronal opiate receptors, was unable to substitute for β-endorphin. Naltrindole, a highly selective δ opiate receptor antagonist, inhibited the action of β-endorphin, whereas a selective μ opiate receptor antagonist was ineffective. Although less potent than β-endorphin, the δ opiate receptor agonist D-Ala2-D-Leu5-enkephalin also significantly enhanced [Ca2+](i) responses. In summary, concentrations of β-endorphin, within the physiological range found in the systemic circulation, modulate the increase in T cell [Ca2+](i) induced by Con A. Both the efficacy of D- Ala2-D-Leu5-enkephalin alone and the antagonism of β-endorphin by naltrindole suggest that a δ-type opiate receptor may mediate these effects.

AB - Intracellular calcium mobilization is an important early event involved in T cell activation. The endogenous opioid peptide β-endorphin is known to modulate immune functions that depend on T cell activation, therefore its effect on intracellular calcium mobilization was investigated. The intracellular calcium concentration ([Ca2+](i)) of T cell-enriched splenocytes was measured by flow cytofluorometric analysis using the calcium- sensitive dye, Fluo-3. By gating on the T cell marker, Thy-1, a 95%-pure population oft cells was identified for study. Cells preincubated with β- endorphin showed significantly enhanced [Ca2+](i) responses to the mitogen, Concanavalin A (Con A). This was detectable with concentrations of β- endorphin as low as 10-13 M; maximal enhancement required 10-10 to 10- 9 M doses. The efficacy of β-endorphin was dependent on the duration of pretreatment. β-Endorphin amplified the Con A-induced increase in [Ca2+](i) by reducing the lag time for the response to Con A and by increasing the mean [Ca2+](i) of the cells. N-Ac-β-endorphin, which shows minimal potency at neuronal opiate receptors, was unable to substitute for β-endorphin. Naltrindole, a highly selective δ opiate receptor antagonist, inhibited the action of β-endorphin, whereas a selective μ opiate receptor antagonist was ineffective. Although less potent than β-endorphin, the δ opiate receptor agonist D-Ala2-D-Leu5-enkephalin also significantly enhanced [Ca2+](i) responses. In summary, concentrations of β-endorphin, within the physiological range found in the systemic circulation, modulate the increase in T cell [Ca2+](i) induced by Con A. Both the efficacy of D- Ala2-D-Leu5-enkephalin alone and the antagonism of β-endorphin by naltrindole suggest that a δ-type opiate receptor may mediate these effects.

UR - http://www.scopus.com/inward/record.url?scp=0029980066&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029980066&partnerID=8YFLogxK

U2 - 10.1210/endo.137.8.8754765

DO - 10.1210/endo.137.8.8754765

M3 - Article

VL - 137

SP - 3386

EP - 3393

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 8

ER -